Dissertation > Medicine, health > Internal Medicine > Systemic disease > Poisoning and chemical damage > Alcohol poisoning

Effect of the Galanthamine on NMDAR2B of Hippocampus Neuron in Acute Alcoholism Rats

Author ZhuLinHua
Tutor WuGuang;CuiSongBiao
School Yanbian University
Course Internal Medicine
Keywords Alcoholism NMDA receptor NMDAR2B galanthamine
CLC R595.6
Type Master's thesis
Year 2009
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Objective: To study the effects of galanthamine on N-methyl-D-aspartic acid receptor 2B (NMDAR2B, NR2B) in the hippocampus (HIP) of acute alcoholism rats.Material and Methods: Total of 60 wistar male rats were randomly divided into control group, ethanol group and glanthamine group, and there were 20 rats in each group. The rats in ethanol group were given by intragastric administration with 50% alcohol (v/v) on the dose of 12ml/kg twice per day, in control group were given by same dose of saline, and in galanthamine group were treated by intragastric administration with the same concentration and dosage of alcohol as in ethanol group and peritoneal injection with 2mg/kg of galanthamine once per day for 7 days. In eighth day of experiment, the rats were sacrificed under etherization, and pathological changes of HIP’s zone of rat were observed by HE-staining, and expression of NR2B in neurons of HIP’s zone by immunohistochemical SABC method.Results: The results observed by histopathology showed that in control group, neurons of HIP’s zone lined up in order, cytoplasm had faint staining, and were no degeneration and necrosis; in ethanol group, nerve cells’ layer was unclear, structure was loose, cell number reduced and part of cells degenerated; in galanthamine group, layer of neurons was comparatively clear and arrangement was comparatively dense, and the cell number increased obviously more than ethanol group. The results detected by Immunohistochemistry for NR2B showed that the cell number with expression of NR2B in the HIP’s zone decreased significantly in the ethanol group than in the control group (41.5±2.5 vs 64.0±1.5, P<0.01), increased in the galanthamine group than in the ethanol group (56.8±2.9 vs 41.5±2.5, P<0.05), and had no difference between the galanthamin and control group (56.8±2.9 vs 64.0±1.5, P>0.05).Conclusions:①Acute alcoholism may relate to down regulation of expression of neuron’s NR2B in HIP’s zone.②The galanthamin has role of protection for neuron in HIP’s zone induced by toxicity of acute alcoholism, and its mechanism may relate to galanthamin up-regulation NR2B expression.

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